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PubMedDate not supplied

Stereospecific and circadian-phase-dependent kinetic behavior of d,l-, l-, and d-propranolol in plasma, heart, and brain of light--dark-synchronized rats.

In light--dark-synchronized male rats, the kinetic behavior of d,l-, l-, and d-propranolol after single (1.78 and 8.89 mg/kg) or multiple drug administration (6 X 8.89 mg/kg) was studied in plasma, heart, and brain both in the light period (L) and in the dark period (D). With either dosage regimen the kinetics of racemic propranolol displayed a temporal dependency, elimination half-lives in plasma, heart, and brain being shorter during D than during L. This was observed with the stereoisomers only after single drug application with no circadian phase dependency at steady-state concentrations. On the other hand, the kinetic behavior of l- and d-propranolol exhibited pronounced stereospecificity in that t1/2 Beta, Vdbeta, plasma clearance, and drug accumulation in heart and brain were greater for l-propranolol than for the d-isomer. Stereospecific differences in t1/2 beta and elimination rate were more pronounced during D. In the light of the flow-dependent hepatic extraction of propranolol it is unlikely that daily variations in microsomal liver enzyme activity are responsible for the chronopharmacokinetics of propranolol. It is assumed that daily variations in liver blood flow, which is more effectively reduced by beta-receptor blockade in the period of increased sympathetic tone during D, are mainly responsible for the chronopharmocokinetics of the therapeutically used d,l-propranolol.

Animals↗
PubMed1986

Celiprolol in the treatment of hypertension: a comparison with propranolol.

A randomized double-blind study compared the antihypertensive efficacy of single daily oral doses of celiprolol 200 or 400 mg to twice daily doses of propranolol 40 or 80 mg in 58 patients with uncomplicated essential hypertension (supine diastolic blood pressure range 95-114 mm Hg). Before treatment there was no significant difference in patient characteristics or in the average systolic or diastolic blood pressures or heart rates between the two groups. Sixty-five percent of the celiprolol group and 56% of the patients randomized to propranolol achieved blood pressure control on the lowest dose of each drug. The mean reductions in the systolic and diastolic pressures at the end of the 4 week titration period were -14/-13 mm Hg for the celiprolol group and -11/-12 mm Hg for the propranolol group. Continued treatment with the same doses of celiprolol and propranolol for a further 8 weeks resulted in blood pressure reductions of -18/14 mm Hg and -8/-9 mm Hg, respectively. In 64% of patients taking celiprolol and in 54% of those taking propranolol the prospective target reduction in supine diastolic blood pressure was achieved, namely a reduction to below 90 mm Hg or a reduction lower after propranolol than after celiprolol; celiprolol reduced the heart rate by an average of 6 bt/min and propranolol by 13 bt/min after 12 weeks treatment (p 0.01). Adverse reactions assessed by patient-volunteered information were similar in character and frequency for both drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1990

Chronic propranolol treatment promotes left ventricular dilation without altering systolic function after large myocardial infarction in rats.

In rats with chronic myocardial infarction (MI), we have examined the effects of prolonged beta-adrenergic blockade with propranolol on left ventricular (LV) performance, weight, and volumes. Sham-operated rats and rats with large MI (greater than 30%) were evaluated. Four groups of rats were studied: control, sham-operated (n = 12); control, MI (n = 12); propranolol (500 mg/L of drinking water)-treated, sham-operated (n = 10); and propranolol treated, MI (n = 10). Treatment was started 3 weeks after coronary ligation. After 5-6 weeks, LV, systemic arterial, and right atrial pressures in addition to aortic blood flow before and during volume loading were measured. LV pressure-volume relations were measured ex vivo. The rats with chronic MI demonstrated expected decreases in LV systolic performance and increased LV end-diastolic and right atrial pressures. Propranolol had no independent effect on LV systolic pressure, LV end-diastolic pressure, resting cardiac index, stressed cardiac index during volume loading, peak developed aortic pressure during aortic occlusion, or ejection fraction index in either sham-operated or infarcted rats; however, heart rate was decreased. LV weight/body weight was 2.17 +/- 0.04 mg/g in control sham-operated rats, which was not different from the propranolol-treated sham-operated rats (2.09 +/- 0.04 mg/g). The LV weight/body weight was increased (p less than 0.01) to 2.21 +/- 0.08 mg/g in the propranolol-treated MI group from 1.94 +/- 0.06 mg/g in the control MI group. The LV pressure-volume relation was not altered by propranolol in the sham-operated rats but was shifted to the right by MI.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1995

Stereoselective vascular effects of the (R)- and (S)-enantiomers of propranolol and atenolol.

All beta-adrenergic antagonists have an asymmetric carbon atom, and most commercially available beta-blockers consist of (R)- and (S)-enantiomers in a fixed 1:1-ratio. The drugs are believed to be contraindicated when peripheral vascular disease exists, presumably due to unopposed alpha-adrenergic vasoconstriction. However, little is known about direct vascular effects of beta-blockers or of stereoselective effects on peripheral arteries. Therefore, we investigated the effects on forearm blood flow (FBF) of brachial artery infusions of the (R)- and (S)- enantiomers of propranolol and atenolol (2, 10, and 50 micrograms/min each) and their inhibitory effects on isoprenaline (Iso)-induced vasodilatation by forearm venous occlusion plethysmography in 12 healthy subjects. Only (R)-propranolol caused an increase in FBF (+21%, p < 0.05), whereas (S)-propranolol and (R)- and (S)-atenolol had no direct effect on peripheral arteries. Vasodilatation induced by Iso was abolished by (S)-propranolol and reduced by (R)-propranolol (-56%, p < 0.05) and (S)-atenolol (-68%, p < 0.05), whereas (R)-atenolol had no effect. Our results indicate that the optically pure (R)- and (S)-enantiomers of propranolol and atenolol do not exert direct vasoconstrictive effects. Furthermore, our results confirm that predominantly (S)-enantiomers have beta-adrenoceptor blocking effects, but they also show that neither the non-beta-blocking (R)-enantiomer of propranolol nor the (S)-enantiomer of the beta 1-selective agent atenolol is completely devoid of blocking effects on vascular beta 2-adrenoceptors.

Adult↗
PubMed1995

Different actions between pindolol and propranolol on the ionic currents in spontaneously beating rabbit sino-atrial node cells.

Electrophysiological effects of beta-adrenoceptor blocking drugs (pindolol and propranolol) on the action potentials (APs) and the membrane currents in spontaneously beating rabbit sino-atrial (SA) node cells were examined by the two-microelectrode voltage-clamp technique. Cumulative administrations of both blocking drugs (10(-7)-10(-6) M) prolonged the AP duration (APD) and caused a negative chronotropic effect in a concentration-dependent manner. Propranolol exhibited stronger responses than pindolol. At 10(-6) M, propranolol depolarized the maximum diastolic potential (MDP) and pindolol decreased the maximum rate of depolarization significantly, but the drugs had little or no effect on the AP amplitude (APA). In voltage-clamp experiments, both blockers (10(-7)-10(-6) M) inhibited the slow inward and the time-dependent outward currents in a concentration-dependent manner. Holding potential was -40 mV. The hyperpolarization-activated inward current was not affected by pindolol, but it was concentration-dependently inhibited by propranolol. The inactivation curve of Isi was not modified by either pindolol or propranolol. The activation curve of IK was unaffected by pindolol, but was shifted by propranolol 10(-6) M by approximately 11 mV in the depolarizing direction. These results indicate that both beta-adrenoceptor blocking drugs (pindolol and propranolol) inhibit the slow inward and the time-dependent outward currents, but produce different actions on the hyperpolarization-activated inward current and the activation kinetic of IK due to their pharmacological properties, thereby resulting in difference in decrease in the spontaneous activity of rabbit SA node cells.

Action Potentials↗
PubMed2001

Haemodynamic effects of propranolol, octreotide and their combination during fasting and post-prandial splanchnic hyperaemia in patients with cirrhosis.

BACKGROUND/AIMS: This double-blind study was designed to evaluate the haemodynamic effect of two drugs, propranolol and octreotide, and their combination in patients with cirrhosis. METHODS: Fifteen patients with cirrhosis were randomly assigned to two groups receiving either octreotide subcutaneously at 100 microg ('octreotide' group, n = 9) or propranolol orally at 40 mg followed by a subcutaneous dose of octreotide (100 microg) after 1 h ('propranolol + octreotide' group, n = 6); then, after 30 min, a standard meal was administered to both groups. The hepatic vein pressure gradient by hepatic vein catheterization, portal and superior mesenteric artery blood flow velocity, superior mesenteric artery pulsatility index by the echo-Doppler duplex system were recorded at baseline, 1 h after propranolol in the 'propranolol + octreotide' group, and in both groups 30 min after octreotide and 30 min after meal. RESULTS: At fast, propranolol was more active in decreasing portal pressure (from 16 +/- 2.2 to 12.7 +/- 3.8 mmHg, -20%, P < 0.05) as compared to octreotide (from 18.6 +/- 4.8 to 16.6 +/- 4.3 mmHg, -11%, P < 0.05). Conversely, octreotide was more active on the mean blood flow velocity of superior mesenteric artery (from 22.8 +/- 5 to 19 +/- 4.5 cm/ s, -17%; P< 0.05). Octreotide administration in patients receiving beta-blockers showed, also, a trend to increase the mesenteric vascular resistances (pulsatility index from 3.14 +/- 0.69 to 3.68 +/- 1.29, +17%, not significant (NS)) which had not been affected by previous treatment with propranolol. After the meal, a reduction of the expected hyperaemic response occurred in both groups. CONCLUSIONS: The combined acute haemodynamic effect of this association suggests the possible combination of these two drugs in critical situations, such as variceal bleeding in patients receiving beta-blockers. The simultaneous use of echo-Doppler and hepatic vein catheterization permitted us a more complete analysis of the acute haemodynamic events.

Adrenergic beta-Antagonists↗
PubMed2005

Endoscopic variceal ligation vs. propranolol for prevention of first variceal bleeding: a randomized controlled trial.

OBJECTIVES: Data in the literature regarding the role of endoscopic variceal ligation for the prevention of first variceal bleeding in cirrhotic patients are controversial. To further explore this issue we have compared ligation and propranolol treatment in a prospective randomized study. METHODS: Sixty patients with cirrhosis and oesophageal varices with no history but at high risk of bleeding were randomized to ligation treatment (30 patients) or propranolol (30 patients). Patients were followed for approximately 27.5 months. RESULTS: Variceal obliteration was achieved in 28 patients (93.3%) after 3+/-1 sessions. The mean daily dose of propranolol was 60.3+/-13.3 mg. Two patients (6.7%) in the ligation group and nine patients (30%) in the propranolol group developed variceal bleeding (P = 0.043). The actuarial risks of variceal bleeding at 2 years were 6.7% and 25%, respectively. On multivariate analysis, propranolol treatment and grade III varices turned out to be predictive factors for the risk of variceal bleeding. Mortality was not different between the two groups. There were no serious complications due to ligation. Propranolol treatment was discontinued in four patients because of side effects. CONCLUSIONS: Variceal ligation is a safe and more effective method than propranolol treatment for the prevention of first variceal bleeding in cirrhotic patients with high-risk varices.

Adrenergic beta-Antagonists↗
PubMed1977

Effect of sodium loading and exercise on renal haemodynamics and urinary sodium excretion in young patients with essential hypertension before and during propranolol treatment.

The effects on renal plasma flow (RPF) and glomerular filtration rate (GFR) of an i.v. sodium load and exercise have been measured in 14 young patients with essential hypertension before and after 3-4 months' treatment with propranolol as well as in 10 normotensive control subjects. In the untreated hypertensive patients, RPF and GFR were significantly reduced during sodium loading and exercise. After propranolol treatment, RPF and GFR were unaffected by sodium loading but decreased during exercise. In the normotensive control group, GFR and RPF were unchanged during sodium loading; RPF decreased during exercise, wherease GFR was not significantly reduced. RPF was significantly lower in the untreated hypertensive patients than in the normotensive control subjects during sodium loading and exercise. Propranolol treatment induced a significant reduction of BP and heart rate. RPF and GFR were not altered by propranolol treatment during sodium loading. During exercise, however, RPF was significantly lower after treatment than before. Urinary sodium excretion during sodium loading was significantly higher in the hypertensive patients than in the control subjects and decreased significantly during propranolol treatment. The reason for the abnormal reduction in renal haemodynamics during sodium loading in patients with essential hypertension is not clarified, but may possibly be related to functional or structural alterations in the renal vascular bed. The lower RPF during exercise after treatment with propranolol is most likely caused by an inhibition of the cardiac output induced by beta-adrenergic blockade. It is conceivable that the reduced urinary sodium excretion during propranolol treatment is attributable to the reduction of BP.

Adult↗
PubMed1975

Comparative trial of propranolol and practolol in hyperthyroidism.

The possible role of practolol in the management of hyperthyroidism has been studied by comparing it with propranolol. 2. In a double-blind cross-over trial, propranolol (40 mg), practolol (120 mg) and a placebo four times daily for one week were compared in twenty-one hyperthyroid patients by sequential analysis. 3. Judged by their effect on the symptoms and signs of thyrotoxicosis, both propranolol and practolol were significantly better than the placebo but no clear distinction could be made between the two active compounds. 4. Propranolol and practolol reduced heart rate by 24 and 17% respectively compared with placebo. 5. Patients generally preferred propranolol or practolol to placebo but this preference did not achieve significance with either drug. 6. Only in its effect on heart rate was practolol significantly inferior to propranolol, and it would appear to be a useful alternative to propranolol in the management of the peripheral manifestations of hyperthyroidism.

Clinical Trials as Topic↗
PubMed1978

Comparative trial of atenolol and propranolol in hyperthyroidism.

1 The use of atenolol, a cardioselective beta-adrenoceptor antagonist, in the management of hyperthyroidism has been studied by comparing it with propranolol. 2 In a double-blind cross-over trial, atenolol (50 mg), propranolol (40 mg) and placebo 4 times daily for 1 week were compared in twenty-one hyperthyroid patients by sequential analysis. 3. Patients generally preferred atenolol or propranolol to placebo but this preference only achieved significance with propranolol. 4 Judged by their effect on the symptoms and signs of hyperthyroidism, both atenolol and propranolol were significantly better than placebo, but no distinction could be made between the two active compounds. 5 Atenolol and propranolol reduced mean heart rate by 29.8 and 27.1% respectively compared with placebo. 6 Atenolol appeared almost equally effective to propranolol in the management of the peripheral manifestations of hyperthyroidism.

Atenolol↗
PubMed1981

Cimetidine increases steady state plasma levels of propranolol.

1 The influence of cimetidine (1000 mg daily) on propranolol steady state plasma levels has been studied in seven normal volunteers. Cimetidine was used as a 200 mg normal release tablet whereas propranolol was given as a 160 mg slow release formulation once daily. 2 After 1 day of cimetidine treatment (day 9 of the study) the mean (Css) and minimal (Css min) propranolol steady state plasma levels increased significantly from 24.1 +/- 14.9 ng/ml (mean +/- s.d.) to 39.2 +/- 27.7 ng/ml (P = 0.01) and from 14.8 +/- 9.3 ng/ml to 27.1 +/- 21.2 ng/ml (P = 0.03), respectively. The apparent oral clearance (Clo) was reduced from 6.7 +/- 4.3 l/min to 4.6 +/- 3.11/min (P = 0.006). 3 A prolongation of cimetidine administration to 5 days (day 13 of the study) intensified this effect significantly (P = 0.02): Css of propranolol was elevated from 23.2 +/- 14.4 ng/ml to 44.9 +/- 26.7 ng/ml (P = 0.003); Css min was increased from 14.1 +/- 10.2 ng/ml to 28.4 +/- 17.9 ng/ml (P = 0.02) while Clo decreased from 6.9 +/- 4.1 1/min to 3.3 +/- 1.61/min (P = 0.006). 4 We conclude that the drug interaction between propranolol and cimetidine leads to significant elevations of propranolol steady state plasma concentrations which may cause a clinically relevant enhancement of the effect of a given dosage. This requires careful observation of patients under concomitant treatment with propranolol and cimetidine.

Adult↗
PubMed1983

Antihypertensive effect of propranolol at rest and during exercise.

In eight patients with normal-renin, moderate hypertension, the antihypertensive effects of increasing doses of propranolol (80, 160, 320 and, in three patients, 640 mg/day, each dose for 2 weeks) were evaluated at rest and during exercise in relation to the degree of beta-adrenoceptor blockade induced. A significant decrease (11 +/- 4 mm Hg) in systolic blood pressure was found after propranolol 80 mg/day. Systolic blood pressure showed a fall of 16 +/- 4 mm Hg after 160 mg/day, but no further decrease was measured at higher doses. Diastolic blood pressure showed a significant drop (by 9 +/- 3 mm Hg) after propranolol 80 mg/day; a decrease by 12 +/- 3 mm Hg after propranolol 160 mg/day, but no further decreases at higher doses. PRA and the rise of systolic blood pressure during bicycle exercise were suppressed to a similar extent by propranolol 80 ng and the higher doses. At 80 mg daily exercise tachycardia was reduced by 18%, at 160 mg by 28%, and at the 2 higher doses by 32%. These results suggest that relatively low doses of propranolol (80-160 mg daily) induce most of the antihypertensive effect of propranolol not only at rest but also during exercise. Complete cardiac chronotropic beta-adrenoceptor blockade may not be necessary for the full hypotensive effect.

Adult↗
PubMed1983

Exercise-induced increments in plasma levels of propranolol and noradrenaline.

Exercise-induced changes in the plasma levels of propranolol and noradrenaline were determined in nine volunteers. Total plasma propranolol levels were increased during submaximal treadmill exercise, with exercise-induced increments of 13 +/- 4% at 4 h after the last dose, 18 +/- 7% at 9 h and 41 +/- 5% at 16 h. Exercise-induced increments in plasma propranolol were observed after single as well as repeated doses. During exercise, increments in plasma propranolol were correlated temporally with changes in plasma noradrenaline. Exercise-induced increments in plasma noradrenaline were greater during propranolol administration than during placebo periods. The changes in plasma propranolol concentration during exercise may reflect a redistribution of propranolol at its site(s) of action.

Humans↗
PubMed1984

The effects of acute or chronic ingestion of propranolol or metoprolol on the physiological responses to prolonged, submaximal exercise in hypertensive men.

We have studied the physiological responses to 50 min of intermittent, moderate exercise in hypertensive men after the ingestion of a single dose of placebo, propranolol or metoprolol, and also after 28 days treatment. In addition, subjective assessments of mood were made during the last 7 days of each period of chronic treatment. Heart rate and blood pressure, both at rest and during exercise, were significantly reduced by a single dose of propranolol or metoprolol; more marked effects were observed after chronic treatment. Ventilation and gas exchange during exercise were only slightly disturbed by single doses of propranolol or metoprolol, whereas chronic treatment had no effect. Perceived exertion scores were increased after a single dose of either drug, compared to placebo, and the effect of propranolol was greater than that of metoprolol. With chronic treatment there were fewer differences between the perceived exertion scores during exercise, although 'leg' fatigue remained greater after propranolol than after placebo. Sweating from the forehead during exercise was enhanced by a single dose of either beta-adrenoceptor antagonist, with propranolol having the greater effect. After chronic treatment the effect of propranolol was diminished, whereas the effect of metoprolol was maintained. Very few disturbances of mood were found after chronic ingestion of the beta-adrenoceptor antagonists.

Adult↗
PubMed1985

The impairment of lignocaine clearance by propranolol--major contribution from enzyme inhibition.

To account for a 40% lowering of the systemic clearance of lignocaine by propranolol treatment it has been proposed that propranolol reduces liver blood flow by 25% and causes a 50% decrease in the intrinsic clearance of lignocaine by enzyme inhibition. In theory, the contribution of direct enzyme inhibition is best evaluated using oral administration of lignocaine when models of hepatic drug clearance predict that propranolol could increase the AUCpo of lignocaine by 100-140%. This hypothesis was tested in six healthy men who received 200 mg lignocaine HCl X H2O orally with and without propranolol pre-treatment (80 mg twice daily for 3 days). Propranolol treatment increased the mean plasma AUCpo of lignocaine by 113 +/- 58 s.d.% (P less than 0.005); it increased the peak plasma lignocaine concentration by 79 +/- 50 s.d.% (P less than 0.025) and it prolonged the elimination half-life of lignocaine by 20 +/- 13 s.d.% (P less than 0.05). Propranolol treatment lowered indocyanine green clearance by 11 +/- 15 s.d.%, but this change was not significant statistically. These experimental results are in accord with the theoretical predictions suggesting that propranolol lowers the systemic clearance of lignocaine mainly by direct inhibition of its metabolism rather than by a lowering of the hepatic blood flow.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Cardiac antiarrhythmic evaluation of naloxone with or without propranolol using a modified chloroform-hypoxia screening test in the rat.

The effects of naloxone and propranolol on cardiac arrhythmias and durations from respiratory arrest to ventricular asystole and cardiac standstill were studied in unanaesthetized young rats induced to suffer respiratory arrest and exhibit ventricular fibrillation (VF) by a modified chloroform hypoxia technique. Both naloxone and propranolol reduced the incidence of VF dose dependently, indicating that they have antiarrhythmic effects. Addition of naloxone to propranolol shifted the dose-response curve of propranolol to the left significantly, indicating an additive effect of the two drugs in their antiarrhythmic activity. Both naloxone and propranolol prolonged the duration from respiratory arrest to ventricular asystole. However, joint administration of both did not further prolong this duration indicating an absence of additive effects. Naloxone prolonged the duration from respiratory arrest to cardiac standstill, indicating that naloxone prolonged the survival time. In contrast, propranolol did not produce the same effect. That naloxone both produced antiarrhythmic effect and prolonged the survival time whereas propranolol only corrected cardiac arrhythmias suggests that the antiarrhythmic effect of naloxone may not result in prolongation of survival time and that different mechanisms may be involved in the antiarrhythmic effect.

Animals↗
PubMedDate not supplied

Does propranolol maintain post-sclerotherapy variceal obliteration? A prospective randomized study.

Variceal recurrence and rebleeding are common after initial obliteration by injection sclerotherapy. To investigate whether propranolol can maintain variceal obliteration by sclerotherapy, 59 patients with oesophageal variceal bleeding after sclerotherapy were enrolled. Patients were allocated to propranolol treatment (30 patients) or served as controls (29 patients). After a mean follow up of 2 years and 4 months, 53 patients completed the study. Fifty-eight per cent of the propranolol group versus 77% of the control group experienced recurrent varices (P = 0.20). Fifteen per cent of the propranolol group versus 11% of the control group developed cardiac varices. Recurrent variceal bleeding was encountered in 27% of the propranolol group and 19% of the control group. Three patients in the propranolol group, compared with two patients in the control group, died of massive variceal bleeding. Eighty per cent of them bled from cardiac varices. Both groups had similar survival rates. We therefore concluded that the use of propranolol after variceal obliteration by sclerotherapy can neither prevent oesophagogastric variceal recurrence nor prevent further rebleeding.

Combined Modality Therapy↗
PubMed2006

Endoscopic variceal ligation versus propranolol in prophylaxis of first variceal bleeding in patients with cirrhosis.

BACKGROUND AND AIM: To compare the efficacy and safety of endoscopic variceal ligation (EVL) with propranolol in prophylaxis on the rate of first esophageal variceal bleeding in patients with cirrhosis. METHODS: A prospective, randomized trial was conducted in 100 cirrhotic patients with no history of previous upper gastrointestinal bleeding and with esophageal varices endoscopically judged to be at high risk of hemorrhage. The end-points of the study were bleeding and death. RESULTS: Life-table curves showed that prophylactic EVL and propranolol were similarly effective for primary prophylaxis of variceal bleeding (11/50 [22%]vs 12/50 [24%]; P = 0.68) and overall mortality (14/50 [28%]vs 12/50 [24%]; P = 0.49). The 2-year cumulative bleeding rate was 18% (9/50) in the EVL group and 16% (8/50) in the propranolol group. The 2-year cumulative mortality rate was 28% (14/50) in the EVL group and 24% (12/50) in the propranolol group. Comparison of Kaplan-Meier estimates of the time to death of both groups showed no significant difference in mortality in both groups (P = 0.86). Patients undergoing EVL had few treatment failures and died mainly of hepatic failure. In the propranolol group, the mean daily dosage of the drug was 68.2 +/- 32.8 mg, which was sufficient to reduce the pulse rate by 25%. 20% of patients withdrew from propranolol treatment due to adverse events. CONCLUSIONS: Prophylaxis EVL is as effective and as safe as treatment with propranolol in decreasing the incidence of first variceal bleeding and death in cirrhotic patients with high-risk esophageal varices.

Adrenergic beta-Antagonists↗